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MBC in Press, published online ahead of print October 17, 2007
Mol. Biol. Cell 10.1091/mbc.E07-05-0460

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Submitted on May 16, 2007
Revised on September 24, 2007
Accepted on October 5, 2007

Caenorhabditis elegans Intersectin: A Synaptic Protein Regulating Neurotransmission

Simon Rose,* Maria Grazia Malabarba,{dagger}{ddagger} Claudia Krag,* Anna Schultz,* Hanako Tsushima,{dagger} Pier Paolo Di Fiore,{dagger}{ddagger}{sect} and Anna Elisabetta Salcini*{dagger}

*Biotech Research and Innovation Centre (BRIC), DK-2200 Copenhagen, Denmark; {dagger}IFOM, the FIRC Institute for Molecular Oncology Foundation, 20139, Milan, Italy; {ddagger}Dipartimento di Medicina, Chirurgia ed Odontoiatria, Universita’ degli Studi di Milano, 20122 Milan, Italy; {sect}European Institute of Oncology, 20141 Milan, Italy

Monitoring Editor: Sandra Schmid

Intersectin is a multifunctional protein that interacts with components of the endocytic and exocytic pathways and is also involved in the control of actin dynamics. Drosophila intersectin is required for viability, synaptic development and synaptic vesicle recycling. Here, we report the characterization of intersectin function in C. elegans. Nematode intersectin (ITSN-1) is expressed in the nervous system, and it is enriched in presynaptic regions. The C. elegans intersectin gene (itsn-1) is nonessential for viability. In addition, itsn-1-null worms do not display any evident phenotype, under physiological conditions. However, they display aldicarb-hypersensitivity, compatible with a negative regulatory role of ITSN-1 on neurotransmission. ITSN-1 physically interacts with dynamin and EHS-1, two proteins involved in synaptic vesicle recycling. We have previously shown that EHS-1 is a positive modulator of synaptic vesicle recycling in the nematode, likely through modulation of dynamin or dynamin-controlled pathways. Here, we show that ITSN-1 and EHS-1 have opposite effects on aldicarb sensitivity, and on dynamin-dependent phenotypes. Thus, the sum of our results identifies dynamin, or a dynamin-controlled pathway, as a potential target for the negative regulatory role of ITSN-1.

Address correspondence to: Anna Elisabetta Salcini (lisa.salcini{at}bric.dk)






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